Just for the Media
SOT 2011 Annual Meeting Information
Science writers, editors, trade press, journalism students, and industry media representatives are cordially invited to attend the Society of Toxicology’s 50th Annual Meeting and ToxExpo™, which is being held March 6–10, 2011, at the
Walter E. Washington Convention Center.
Please complete the Mail/Fax
registration form and you will be entitled to a complimentary registration to this five-day event. Members of the media may also register on-site at the Walter E. Washington Convention Center. If you choose to register on-site, please be sure to bring your press credentials to registration.
For more information about the SOT Annual Meeting contact Martha Lindauer.
Information for the News Media
Welcome to the Society of Toxicology’s media information page. This page is designed to provide the news media with information about various scientific sessions that will take place at the Society of Toxicology’s 50th Anniversary Annual Meeting on March 6–10, 2011, at the Walter E. Washington Convention Center in Washington, D.C.
The Society of Toxicology 50th Annual Meeting and ToxExpo features a number of topical presentations that the news media will find newsworthy. The following provides an overview of some of the most newsworthy and timely sessions.
If you are a member of the news media and interested in attending any of the below sessions, you can contact our communications staff to assist with your needs. Staff members are available during the hours of Monday–Friday, 8:30 AM to 5:00 PM Eastern. The Society of Toxicology will have a press room at the Walter E. Washington Convention Center in Washington, D.C. for members of the news media who attend the Annual Meeting. The Society of Toxicology’s Communications Department will field calls and set up interviews for reporters with any of the panelists who are participating in the Annual Meeting.
Media Contact Information
Exhibitor Hosted Session
U.S. EPA Special Session on New Clean Air Research Centers
Monday, March 7, 2011
3:30 PM–4:30 PM
Room 140B Convention Center
The U.S. Environmental Protection Agency (U.S. EPA) will present its newly funded Clean Air Research Centers, based at leading research universities. The center directors and Dan Costa, Ph.D., U.S. EPA’s Interim Director for Air, Climate, and Energy, will discuss the future of air pollution research and new cutting edge research under way to better understand the role of air pollution mixtures in human health risks.
Historical Highlights Session
50 Years of “the Pill”: Risk Reduction and Discovery of Benefits beyond Contraception
Wednesday, March 9, 2011
6:30 AM–7:50 AM
Room 147 Convention Center
As with many drug firsts, several lessons can be learned from the oral contraceptive in terms of its development and use. Indirectly, “the Pill” played a significant role in reshaping pharmacology, social perceptions of medication, and the regulatory process for new drugs during the second half of the 20th century. Recent scientific and technological advances in genomics, proteomics, new materials, and new drug delivery systems, along with a new understanding of reproductive biology, offer the promise of new, safe, and effective forms of contraception. Another area of research interest involves the exploration of some novel approaches to male contraception that requires identification of “novel” proteins for male reproduction. Presenters will revisit the implications of administering a drug to women who are not sick, how the drugs have been modified based on safety concerns, and the emergence of health benefits separate from those related to reproduction.
Kristina D. Chadwick, Bristol-Myers Squibb, New Brunswick, NJ, “The Pill”: Historical Overview 1961–2011
Ronald T. Burkman, Baystate Medical Center, Springfield, VA, Oral Contraceptives: A 50 Year Experience of Overall Cardiovascular Safety
Belen M. Tornesi, Novel Approaches for Contraception: Reflections and Forecast
Toxicological Considerations in the Gulf of Mexico Oil Spill
Monday, March 7, 2011
2:00 PM–4:45 PM
The Deepwater Horizon oil rig explosion of April 20, 2010, resulted in the release of millions of gallons of petroleum crude oil into the Gulf of Mexico waters. The major ecological effects will be described and compared to the normal Gulf ecosystem dynamics. The types of and likelihood of possible human adverse health effects, both acute and latent will be presented in light of what is known of the exposure routes and the conditions. Panelists will look at dispersants and the short-term health effects from oil spills and as well critical information needs.
M. C. Madden, U.S. EPA, Chapel Hill, NC, Toxicological Considerations in the Gulf of Mexico Oil Spill
W. Benson, S. Jordan, R. Greene, V. Engle, M. Hemmer, and M. Barron, Gulf Ecology Division, U.S. EPA, Gulf Breeze, FL, The Gulf of Mexico Ecosystem: Consequences of the BP Oil Spill
J. Michel, Research Planning Inc., Columbia, SC, The Fate, Behavior, and Weathering of Spilled Oil from the Deepwater Horizon Spill
L. Mitchelmore, Center for Environmental Science, University of Maryland, Solomons, MD, Oil Spill Chemical Dispersants: The Good, The Bad, or The Ugly?
N. Sathiakumar, University of Alabama, Birmingham, Birmingham, AL, Short-Term Health Effects from Oil Spills
W. H. Farland, Colorado State University, Ft. Collins, CO, Risk Assessment of the Spill: Critical Information Needs
Developmental Origins of Adult Disease: The Effects of Low-Dose Lead (PB)
Tuesday, March 8, 2011
1:30 PM–4:15 PM
Prenatal exposure of lead at low, environmentally-relevant doses causes physiological changes that increase the likelihood of diseases in adulthood such as obesity, hypertension, and neurological disorders. Panelists will discuss experimental animal toxicology data that suggest several possible sources for developmental origins of adult’s diseases.
E. P. Hines, A. Rooney, U.S. EPA, Research Triangle Park, NC
Developmental Origins of Adult Disease: The Effect of Low-Dose Lead
D. A. Fox, University of Houston, Houston, TX
Low-Level Gestational Lead Exposure Is a Risk Factor for Late-Onset Metabolic Syndrome and Neurodegeneration
D. A. Cory-Slechta, Dept. of Environmental Medicine, University of Rochester, Rochester, NY
Developmental Lead (PB) Exposure and Permanent HPA Axis Dysfunction: A Potential Unifying Biological Mechanism for PB-Associated Diseases and Disorders
N. Zawia, Biomedical Sciences, University of Rhode Island, Kingston, RI
Early Life Exposure to PB and Programmed Susceptibility to Neurodegenerative Disease
A.Rooney, Center for the Evaluation of Risks to Human Reproduction, NIEHS, National Toxicology Program, Research Triangle Park, NC
Contrasting the Developmental and Adult Origins of Adverse Effects from Lead in the Draft NTP Monograph on Low-Level Lead
Does the Clock Make the Poison? Influence of the Circadian Clock on Toxicological Mechanisms and Outcomes
Tuesday, March 8, 2011
1:30 PM–4:15 PM
Everyone’s biochemical, physiological, and behavioral activities are synchronized by light/dark cycles. These fluctuations are maintained by the circadian clock, which has intrinsic periodicity of approximately 24 hours. Environmental and occupational exposure leading to disruption of the circadian rhythm, including jet lag, light-at-night and shift work are associated with increased risk of cancer, cardiovascular disease, diabetes, obesity, reproductive problems, sleep disorders, drug and alcohol addiction, and psychiatric disorders. Presenters will provide an overview of this emerging area of concern and talk about opportunities for disease prevention.
H. Zarbl, Environmental and Occupational Health Sciences Institute, Robert Wood Johnson Medical School, Piscataway, NJ and L. A. Hooven, Dept. of Zoology, Oregon State University, Portland, OR, Does the Clock Make the Poison: Influence of the Circadian Clock on Toxicological Mechanisms and Outcomes
U. Schibler, Molecular Biology, University of Geneva, Geneva, Switzerland, Environmental Influences Uncouple Peripheral Clocks from SCN Clocks
D.J. Earnest, Neuroscience and Experimental Therapeutics, Texas A&M Sciences Center, College Station, TX, Tick-Toxicology: Clock Gene Expression and Interactions Between the Molecular Pathways for the Regulation of Circadian Rhythms, and Toxin Metabolism
C. A. Bradfield, J. A. Walisser, B. P. Johnson, Y. Liu, A. Shen, E. L. McDearmon, B. McIntosh, A. Vollrath, the McArdle Laboratory for Cancer Research, University of Wisconsin School of Medicine and Public Health, Madison, WI; A. C. Schook and J. S. Takahashi, Northwestern University, Evanston, IL, The Hepatocyte Autonomous Clock Modulates the Chronotoxicity of Acetaminophen
C. D. Klaassen, Pharmacology, University of Kansas Medical Center, Kansas City, KA, Circadian Expression of Drug Processing Genes in Mice
M. Fang and H. Zarbl, Environmental and Occupational Health Sciences Institute, Robert Wood Johnson Medical School, Piscataway, NJ, Methylselenocysteine Resets the Rhythmic Expression of Circadian and Growth Regulatory Genes Disrupted by Nitrosomethylurea In Vivo
Autism: Genetic, Epigenetic, and Environmental Factors Influencing Neural Networks
Wednesday, March 9, 2011
9:00 AM–11:45 AM
Autism is a complex developmental disability that typically appears during the first three years of life and affects a person’s ability to communicate and interact with others. Autism is defined by a certain set of behaviors and is a “spectrum disorder” that affects individuals differently and to varying degrees. In December 2009, the Centers for Disease Control and Prevention issued their ADDM autism prevalence report, that concluded that the prevalence of autism had risen to 1 in every110 births in the United States and almost 1 in 70 boys. The cost to treating autism and autism spectrum disorders (ASD) has increased astronomically.
A major controversy continues to be focused on whether ASDs have a purely genetic cause. Although ASDs have high heritability, the underlying genetics is extremely complex with no one gene fully accounting for the disorder. Many environmental factors ranging from demographic, to chemical exposure, to nutrition, to vaccinations have been proposed to contribute to ASD risk, yet none are proven. From a toxicologist’s point of view, the identity of defective genes and signaling pathways linked to autism provide important clues about exposures to environmental chemicals that influence autism susceptibility, severity, and/or treatment. Panelists will review current knowledge of genetic contributions to autism risk and present recent findings that show how impairments in neural connectivity contribute to autism.
N. Pessah, Dept. of Molecular and Biological Sciences, University of California at Davis, Davis CA, Autism: Genetic, Epidenetic, and Environmental Factors Influencing Neural Networks
S. B. Selleck, Biochemistry and Molecular Biology, the Pennsylvania State University, University Park, PA, Copy Number Burden Associated with Autism in Unstable Segments of the Genome
R. O. Vallero, Microbiology and Immunology, University of California at Davis, Davis, CA, Epigenetic Interaction Between Perinatal PBDE Exposure MECP2308 Mutation Through X Chromosome Inactivation
P. Levitt, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, Pathogenesis of circuit Development in the Autisms: Emergence of the Gene-Environment and the Developmental Neurobiology Interface
C. Lawler, Division of Extramural Research and Training, NIEHS, Research Triangle Park, NC, Autism and the Environment: Challenges and Opportunities for Advancing the Science
Risk Assessment for Proteins Induced into Genetically Modified Crops
Tuesday, March 8, 2011
1:30 PM–4:15 PM
In 2009, there was 330 million acres of genetically modified crops planted in 25 countries. While genetically modified crops are widely grown in the U.S., Canada and Latin American, they remain controversial in Europe and parts of Asia. The president of Zambia rejected food aid from the U.S. for his country in the midst of a famine as he was counseled that the genetically modified food aid was poisonous. In some parts of the world, there is not enough credible information to allow the public to make an informed decision. There is also a lack of basic understanding of science among the people. Panelists will address some of the scientific issues that have been raised about the use of biotechnology to generate new varieties of food crops and panelists will focus on the safety assessment of proteins introduced into food crops to impart the intended change to the plant.
B. G. Hammond, Product Safety Center, Monsanto Company, St. Louis, MO, Risk Assessment for Proteins Introduced into Genetically Modified (GM) Crops
J. M. Jez, The Donald Danforth Plant Science Center, St. Louis, MO, Nature’s Balancing Act: Evolutionary Changes in Protein Families
S. J. Franklin Protein Technologies, Monsanto Co., Cambridge, MA, Engineering Proteins to Improve Biological Function
J. L. Kough, Biopesticides and Pollution Protection Division, Office of Pesticide Programs, U.S. Environmental Protection Agency, Washington, D.C., Safety Assessment of Novel Proteins
H. A. Kuiper, European Food Safety Agency, Parma, Italy, EFSA’s Updated Strategy for the Risk Assessment of GM Plants and Derived Food/Feed
B. G. Hammond, Product Safety Center, Monsanto Co., Saint Louis, MO, Risk Assessment Recommendations for Introduced Proteins
Role of Biomarkers in Assessing Tobacco Harm Reduction: A Toxicological Perspective
Thursday, March 9, 2011
9:00 AM–11:45 AM
Tobacco is a leading cause of death and disease, and smoking remains the single most important public health issue in the United States. Tobacco companies have marketed a number of products including light cigarettes, smokeless cigarettes and oral tobacco products that are perceived by the public as being less harmful than regular cigarettes. The potential for these products to reduce exposure and harm have yet to be tested. Panelists will focus on four research areas that are critical for any harm reduction strategy and these include: (1) measuring the levels of nicotine or carcinogens in tobacco smoke, understand how the design of tobacco products, such as ventilation or filter design, influence the smoke coming from the product, (2) measuring tobacco chemicals, byproducts of smoking, or other biomarkers in smokers’ bloodstreams to understand what chemicals people are inhaling, (3) develop a risk analysis framework in which to assess the mode of toxic action by tobacco smoke components; and (4) develop experimental and computational modeling approaches to determine the relative risk for various tobacco smoke components.
C. Timchalk and R. Corley, Pacific Northwest National Laboratory, Richland, WA, Role of Biomarkers in Assessing Tobacco Harm Reduction: A Toxicological Perspective
M. Zeller, Pinney Associates, Bethesda, MD, Legislative and Regulatory Overview
D. L. Ashley, Center for Tobacco Products, U.S. Food and Drug Administration, Rockville, MD, Association Between the Design, Contents, Emissions, Use and Biomarkers of Exposure from , Tobacco Products
S. S. Hecht, J. Yuan and D. K. Hatsukami, Masonic Cancer Center, University of Minnesota, Minneapolis, MN, Tobacco Carcinogen and Toxicant Biomarkers: Potential Applications in Tobacco Harm Reduction and Regulation
A.R. Boobis, Centre for Pharmacology and Therapeutics, Imperial College London, London, UK, Mode of Action: Assessment of Cancer Risk and Identification of Key Data Needs
C. Timchalk, J. G. Teeguarden and R. A. Corley, Battelle Pacific Northwest Division, Richland, WA, Quantitative Risk Assessment: A Computational Dosimetry Framework for Tobacco Harm Reduction
Protein Aggregation as a Common Mechanism of Toxicity in Neurodegenerative Diseases
Monday, March 7, 2011, 2:00 PM–4:45 PM
Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, Huntington disease, prion diseases and amyotrophic lateral sclerosis (ALS) afflict millions of people and in each of these diseases, aggregation of various disease-specific proteins appears to play a primary role in the pathology. Recent discoveries in the last few years have greatly advanced our understanding of this important neurotoxic mechanism. Panelists review these discoveries and talk about how they open up new avenues for research.
G.W. Miller, Environmental Health, Emory University, Atlanta, GA, Protein Aggregation and Neurodegeneration
S.L. Ackerman, Jackson Laboratory, HHMI, Bar Harbor, ME, Protein Misfolding and Neurodegeneration
M. Lee, University of Minnesota, Minneapolis, MN, Protein Aggregation in Alzheimer’s Disease and Parkinson’s Disease
J. Ma, Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH, The Role of Lipid-Protein Interaction in the Pathogenesis of Prion Disease
A.Kanthasamy, C. Choi, D. Martin, V. Anantharam, J.A. Richt and A. Kanthasamy, Biomedical Sciences, Iowa State University, Ames, IA, Role of Divalent Metals in Prion Protein Upregulation and Aggregation
Disease Prevention: The Next Fifty Years
Monday, March 7, 2011
9:15 AM–12:00 NOON
As the Society of Toxicology embarks on its next fifty years, new opportunities and challenges will no doubt change the role of toxicology in improving human health. High-throughput genomic technologies are increasingly providing mechanistic insights into how exposure to toxicants interacts with other exposures, genetic background, diet, lifestyle, co-morbid disease and numerous other factors to adjust the disease risk. Panelists will explore these emerging technologies and offer a roadmap for increasing the role of mechanistically-based toxicology and ‘omics in disease prevention.
H. Zarbl, Environmental and Occupational Health Sciences Institute, Robert Wood Johnson Medical School, Piscataway, NJ, Disease Prevention: The Next 50 Years
I.Rusyn, Environmental Science and Engineering, University of North Carolina at Chapel Hill, Chapel Hill, NC, Assessing the Impact of Interindividual Genetic Variability on Toxicity Through Toxicogenomic Data
C.P. Wild, International Agency for Cancer Research, Lyon, France, Combining the Genome with Its Exposome for Mechanistically-Based Disease Prevention
M. Smyth, University of California at Berkeley, Berkeley, CA, Top-Down Exposomic Strategies to Characterize the Human Exposome
D. Jones, Emory University, Atlanta, GA, High-Throughput Metabolomics for Identification of Quantitative Exposure and Biomarkers
E. Holmes, Imperial College, London, UK, Role of the Human Microbiome in Human Environmental Exposure and Disease Prevention
J. D. Groopman, Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD, Public Health Opportunities and Challenges in Disease Prevention
Reforming the Toxic Substances Control Act Reform: Challenges, Opportunities and Timing
Monday, March 7, 2011
12:10 PM–1:30 PM
The Toxic Substances Control Act (TSCA) is now 35 years old, and unlike most of the major environmental laws passed in the 1970s, the TSCA legal framework remains essentially unchanged. Achieving the goals of TSCA, namely to ensure that adequate data are available to allow assessment of the effect of chemical substances and mixtures on health and the environment, have also proven difficult. While once a model regulation for other nations, the TSCA framework has not been superseded by safety regulations adopted by other jurisdictions. Issues that are likely to be addressed by reform of TSCA include the distinct toxicology and exposure scenarios posed by nanotechnology and consideration for special populations such as children and those with susceptibilities or chronic health conditions. Panelists will explore the challenges, and opportunities of reforming this 35 year-old statute.
T. Lewandowki and S. Barone, Gradient, Seattle, WA, Reforming the Toxic Substances Control Act (TSCA): Challenges, Opportunities and Timing, Thomas Lewandowski, Gradient, Seattle, WA, Time for Change
Tala Henry, U.S. Environmental Protection Agency, Washington, D.C., U.S. EPA’s Enhanced Chemical Management Program
George Rusch, Honeywell International, Inc., Morristown, NJ, “TSCA Reform and Reach: What We Can Learn and What We Need to Avoid”
James Votaw, Counsel, WilmerHale, Washington, D.C., Legislation for TSCA Reform: The Possible and the Probable
Regional Interest Session
Bombs in Our Backyards? Historical Military Activities and Current Public Health Issues in the U.S. Capital Region
Tuesday, March 8, 2011, 9:00 AM–11:45 AM, Room 150
Unexploded Ordinances (UXO), products of military activities during World War I and World War II, pose a serious threat from detonation and can contain chemical weapons such as sulfur mustard, and nerve gases. The discovery of bombs in the U.S. Capital region, especially in the neighborhood of Spring Valley, has raised several important concerns for area residents for the past 15 years. There are been several phases of investigation about this area and panelists will explore the environmental risks, munitions and explosives of concern in that area, and the toxicity of explosives that have been discovered there. Panelists will also talk about a public health approach to this legacy from World War I.
E. R. Janus, Steptoe & Johnson LLP, Washington, D.C. and L.E. Roszell, Environmental Health Risk Assessment, Aberdeen Proving Ground, MD, A Brief Introduction to Uxo in the Capital Region: Session Overview
D. G. Noble, Baltimore District, U.S. Army Corps of Engineers, Baltimore, MD, Environmental Risk Issues Associated with a Munitions Response Site in Northwest Washington, D.C. The Spring Valley Formerly Used Defense Site
P. Greene, U.S. Army Corps of Engineers, Baltimore, MD, Munitions and Explosives of Concern in Spring Valley and the Washington, D.C. Area
C. Opdyke, Baltimore District, U.S. Army Corps of Engineers, Baltimore, MD, Toxicity of WWI Era Chemicals Studied at Spring Valley, Washington, D.C.
M.A. Fox, Health Policy and Management, Johns Hopkins University, Baltimore, MD, A Public Health Approach to a WWI Legacy: Tracking Health and Environment in Spring Valley
L. Siegel, Center for Public Environmental Oversight, Mountain View, CA, The Role of Trust at Munitions/Chemical Weapons Sites
L.S. Geckle, Health Risk Communication Program, U.S. Army Public Health Center, Aberdeen Proving Ground, MD, Addressing Pubic Perceptions: Communicating Public Health Issues Effectively
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